摘要:

AbstractThe rat liver rhodanese (thiosulphate: cyanide sulfurtransferase EC 2.6.1.1) has been immobilized on polyacrylamide gels. The immobilized enzyme had a pH optimum of 7.4 and Km values of 3.25 mM and 1.12 mM for S2O2−3and KCN, respectively. The enzyme was competitively inhibited by NaNO2and CH3COONa and noncompetitively by amyl‐nitrite. A modulation of activity was observed in the presence of Ca2+, Zn2+, and Cu2+. The results are discussed in line with the detoxicating function of liver rhodan

ISSN:0887-2082    

DOI:10.1002/jbt.2570080202

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractWhen bovine kidney mitochondria were assayed in the presence of Triton X‐100, they were found to contain glycine N‐acyltransferase activity toward the CoA‐adducts of benzoate, butyrate, isovalerate, naphthylacetate, phenylacetate, and salicylate. Heptanoyl‐CoA activity was masked by high acyl‐CoA hydrolase activity. All activities found in detergent‐lysed mitochondria, and also that toward heptanoyl‐CoA, could be released in soluble form by repeated cycles of freeze‐thawing. Activity in the particle‐free lysate decreased in the order: phenylacetyl‐CoA>benzoyl‐CoA>salicylyl‐CoA>butyryl‐CoA>naphthylacetyl‐CoA>heptanoyl‐CoA>isovaleryl‐CoA. This is quite different from liver, where the activity toward the arylacetic acids is much lower and the other activities are higher. This reflects a major difference in the relative expression of the aralkyl and arylacetyl transferases between liver and kidney. The phenylacetyl‐CoA and naphthylacetyl‐CoA activity purified with a single protein which is termed the arylacetyl transferase. This enzyme was similar to the hepatic arylacetyl transferase in terms of its sensitivity to sulfhydryl reagents, response to cations, and molecular weight (33,500). Activity toward benzoyl‐CoA also purified as a single form which was similar to the hepatic form in its molecular weight (34,000), response to cations, and kinetic properties. Conditions leading to the inhibition of this kidney form and also the hepatic fo

ISSN:0887-2082    

DOI:10.1002/jbt.2570080203

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractTo understand the basic mechanisms of TCDD's action to cause hypoinsulinemia in several experimental animals, we have studied TCDD‐induced changes in various protein kinase activities in membrane preparations of guinea pig pancreas. For this purpose, young male guinea pigs were treated through a single intraperitoneal in jection with 1 or 3 μg/kg of TCDDin vivo, and, after given time periods, pancreas samples were obtained and membranes were isolated through homogenization and centrifugation procedures. Several sets of incubation conditions were selected for protein kinase activity assay, each favoring a specific type of protein kinase. It was found that overall protein phosphorylation activities were higher in the preparation from TCDD‐treated an imals as compared to those found in pair‐fed controls and that this trend was more pronounced when the assay medium contained Mn2+in place of Mg2+and EGTA. These are the conditions that are known to favor protein tyrosine kinases. Other types of protein kinases from the treated animals did not show any significant differences from the pair‐fed control animals, though that of protein kinase C in the treated preparation showed a modest increase. To establish that the type of protein kin ases stimulated by TCDD are protein tyrosine kin ases, we have carried out phosphoamino acid analyses, KOH digestion, and western blot analyses using an antibody to phosphotyrosine. All the results were consistent in supporting the idea that TCDD causes a rise in protein‐tyrosine kinases in pancreas at early stages of

ISSN:0887-2082    

DOI:10.1002/jbt.2570080204

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractD. melanogaster development was markedly retarded and its survival decreased by larvae treatment with compounds being strong inducers of the cytochrome P‐450 2B in mammals— phenobarbital (PB*), perfluorodecaline (PFD), transstilbene oxide (TSO), and triphenyldioxane (TPD). At the same time, the weak inducer hexobarbital or the selective cytochrome P‐450 inducer in mice but not in rats 1,4‐bis[2‐(dichloropyridyl‐oxy)]‐benzene (DPB) did not affect the larvae development. The cytochrome P‐450 1A1 inducers benzo(a)anthracene (BA) and β‐naphtoflavone (BNF) were also not effective. The toxicity of phenobarbital was shown to be decreased by the cytochrome P‐450 inhibitor piperonyl butoxide by adding 20‐hydroxyecdysone or by treatment with aminophylline—the indirect enhancer of ecdysone production in the larval prothoracic gland. The hypothesis of the moulting hormone degradation as the cause of elevated larvae mortality resulting from the induced high mixed function oxidase act

ISSN:0887-2082    

DOI:10.1002/jbt.2570080205

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractAn in situ (explant tissue culture) model has been developed to study the effect of 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin (TCDD), hormones, and growth factors either alone or in combination. In our model system, the effect of TCDD on protein phosphorylation was greatly affected by the presence or the absence of externally added D‐glucose. In the presence of a physiologically relevant level of glucose (13.3 mM), TCDD clearly stimulated protein phosphorylation as in the case of in vivo data. However, in the absence of Dglucose TCDD clearly inhibited protein phosphorylation. On the other hand, TCDD reduced the glucose uptake activity in isolated adipose tissue either in the presence or absence of D‐glucose (13.3 mM). Therefore, the TCDD‐induced reduction of glucose transport does not appear to be related directly to the simultaneous rise in protein phosphorylation. For comparison, several agents which are known to affect protein phosphorylation were tested. These hormonal agents generally affected the TCDD‐untreated adipose tissues in the manner expected from their known actions, indicating that this in situ model is an adequate system to study their independent actions. The TCDD‐treated adipose tissue samples showed only mild or insignificant response to these hormonal stimuli. In terms of the changes in the pattern of protein phosphorylation activities, the action of TCDD appeared to resemble that of EGF and T3. Since under in situ conditions no agents such as EGF or T3 can be expected to be present, the observed TCDD‐induced changes are suggestive of the basic intracellular changes in cellular activities. The types of TCDD‐induced protein kinases appear to be protein tyrosine kinases a

ISSN:0887-2082    

DOI:10.1002/jbt.2570080206

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractExcretions of the lipid peroxidation products, formaldehyde (FA), acetaldehyde (ACT), malondialdehyde (MDA), and acetone (ACON), were simultaneously identified and quantitated in the urine of female Sprague‐Dawley rats by gas chromatography‐mass spectroscopy (GC‐MS) and high pressure liquid chromatography (HPLC) following the acute administration of carbon tetra‐chloride, a model alkylating agent that does not induce glutathione depletion, and the redox cycling compounds paraquat and menadione. All three xenobiotics are well‐known inducers of oxidative stress. Oxidative stress was induced by oral administration of single doses of 2.5 mL of carbon tetrachloride/kg, 60 mg menadione/kg, and 75 mg paraquat/kg. These doses are approximately 50% of the LD50's for the three xenobiotics. Urinary excretion of FA, ACT, MDA, and ACON increased relative to control animals following treatment with all xenobiotics. Over the 48 hours of the study, the greatest increases in the excretion of MDA, FA, ACT, and ACON occurred after paraquat administration, with increases of approximately 2.7‐, 2.6‐, 4.3‐, and 11.0‐fold, respectively. This technique may have wide‐spread applicability as an effective biomarker for investigating altered lipid metabolism in disease states and exposure to environmental pol

ISSN:0887-2082    

DOI:10.1002/jbt.2570080207

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

摘要:

AbstractThe reaction of phosgene with ni‐trone spin traps was investigated using electron paramagnetic resonance (EPR)/spin trapping techniques. Evidence for the intermediacy of a carba‐moyl monochloride intermediate was obtained. Isotopic substitution of13C‐phosgene was employed to verify the hyperfine coupling constant assignments. The implications of these observations on pulmonary damage caused by inhalation of phosgene are ment

ISSN:0887-2082    

DOI:10.1002/jbt.2570080208

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY

ISSN:0887-2082    

DOI:10.1002/jbt.2570080201

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1993

数据来源: WILEY